The study of ocular anaphylaxis in rats will be continued. The reaction is defined as an acute inflammatory response of the ocular tissues caused by immunologically induced release of chemical mediators. The three components necessary for anaphylaxis (homocytotropic antibody, mast cells or basophils, and chemical mediators) will be studied in ocular tissues in vivo and in vitro. The test animals will be rats immunized so as to favor IgE antibody production by infection with the nematode Nippostrongylus brasiliensis or immunization with minute amount of egg albumin in alum. We will continue to develop an in vivo model of local ocular anaphylaxis by both local challenge by injection and by topical application of antigen in the antigen in the actively and in the passively sensitized rat. The time course of anaphylaxis, as determined by increased vascular permeability, degranulation of mast cells, and release of histamine into the tissue, will be determined for both the acute and late phases of the reaction. The histologic changes of acute, late-phase, and chronic ocular anaphylaxis will be evaluated. The antibody and cellular requirements will be assessed. The ability of anaphylaxis to increase the release of ocular goblet cell mucus will be evaluated in the local and systemic ocular anaphylaxis models. Increased vascular permeability will be evaluated by measuring 125I-rat serum albumin extravasated into tissue. Mast cell degranulation will be judged on glutaraldehyde-fixed, Epon-embedded, l micron thick, Giemsa-stained tissues. Histamine will be determine by enzymatic isotopic assay. Release of mucus will be determined by radioactive counts of 35S label of goblet cell mucus. The proposed research addresses an area where little data are available. It would provide a contribution to our knowledge of an immunologic mechanism fundamental to the production of ocular inflammation.